Nanotechnology may do the trick, but big pharmaceutical companies are far from embracing that strategy. In the meantime, highly-engineered biological molecules will fill the void.                                                    

Antibodies can recognize cancer cells, and latch onto them, but they won’t kill their targets without some help.

By attaching powerful poisons onto the cancer-seeking antibodies, scientists can make smart drugs that hit diseased cells hard.

When injected into the body, the Y-shaped molecules drift around until they latch onto abnormal cells, and then their toxic payloads kill them. But it turns out that they also cause quite a bit of collateral damage — like liver and kidney irritation.

Researchers at Genentech have found a way to reduce those side effects.

William Mallet, Jagath Junutula, and their colleagues invented a trick to precisely control how many of the cell-killing compounds become bonded to each antibody, and then they tested the carefully crafted drugs on mice, rats and monkeys.

In the current issue of Nature Biotechnology, Mallet and Junutula explain that attaching lots of toxic molecules onto each antibody is not the best idea. One or two poison molecules per protein will suffice.

Image: National Library of Medicine

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Now scientists know why. According to a study released Wednesday, the egg-laying critter is a genetic potpourri — part bird, part reptile and part lactating mammal.

The task of laying bare the platypus genome of 2.2 billion base pairs spread across 18,500 genes has taken several years, but will do far more than satisfy the curiosity of just biologists, say the researchers.

“The platypus genome is extremely important, because it is the missing link in our understanding of how we and other mammals first evolved,” explained Oxford University‘s Chris Ponting, one of the study’s architects.

“This is our ticket back in time to when all mammals laid eggs while suckling their young on milk.”

Native to eastern Australia and Tasmania, the semi-aquatic platypus is thought to have split off from a common ancestor shared with humans approximately 170 million years ago.

The creature is so strange that when the first stuffed specimens arrived in Europe at the end of the 18th century, biologists believed they were looking at a taxidermist’s hoax, a composite stitched together from the body of a beaver and the snout of a giant duck.

But the peculiar mix of body features are clearly reflected in the animal’s DNA, the study found.

The platypus is classified as a mammal because it produces milk and is covered in coat of thick fur, once prized by hunters.

Lacking teats, the female nurses pups through the skin covering its abdomen.

But there are reptile-like attributes too: females lay eggs, and males can stab aggressors with a snake-like venom that flows from a spur tucked under its hind feet.

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The bird-like qualities implied by its Latin name, Ornithorhynchus anatinus, include webbed feet, a flat bill similar to a duck’s, and the gene sequences that determine sex. Whereas humans have two sex chromosomes, platypuses have 10, the study showed.

“It is much more of a melange than anyone expected,” commented Ewan Birney, who led the genome analysis at the European Bioinformatics Institute in Cambridge.

The animal also possesses a feature unique to monotremes — an order including a handful of egg-laying mammals — called electroreception.

With their eyes, ears and nostrils closed, platypuses rely on sensitive electrosensory receptors tucked inside their bills to track prey underwater, detecting electrical fields generated by muscular contraction.

“By comparing the platypus genome to other mammalian genomes, we’ll be able to study genes that have been conserved throughout evolution,” said senior author Richard Wilson, a researcher at Washington University.

In captivity, platypuses have lived up to 17 years of age.

In the wild, they feed on worms, insect larvae, shrimps and crayfish, eating up to 20 percent of their body weight every day.

Males grow to a length of 50 centimetres (20 inches) and weigh about two kilos (4.5 pounds), with females about 20 percent shorter and lighter.

The genome sequenced for the study belongs to a female specimen from New South Wales nicknamed Glennie and can be accessed at www.ncbi.nih.gov/Genbank.

Now scientists know why. According to a study released Wednesday, the egg-laying critter is a genetic potpourri — part bird, part reptile and part lactating mammal.

The task of laying bare the platypus genome of 2.2 billion base pairs spread across 18,500 genes has taken several years, but will do far more than satisfy the curiosity of just biologists, say the researchers.

“The platypus genome is extremely important, because it is the missing link in our understanding of how we and other mammals first evolved,” explained Oxford University‘s Chris Ponting, one of the study’s architects.

“This is our ticket back in time to when all mammals laid eggs while suckling their young on milk.”

Native to eastern Australia and Tasmania, the semi-aquatic platypus is thought to have split off from a common ancestor shared with humans approximately 170 million years ago.

The creature is so strange that when the first stuffed specimens arrived in Europe at the end of the 18th century, biologists believed they were looking at a taxidermist’s hoax, a composite stitched together from the body of a beaver and the snout of a giant duck.

But the peculiar mix of body features are clearly reflected in the animal’s DNA, the study found.

The platypus is classified as a mammal because it produces milk and is covered in coat of thick fur, once prized by hunters.

Lacking teats, the female nurses pups through the skin covering its abdomen.

But there are reptile-like attributes too: females lay eggs, and males can stab aggressors with a snake-like venom that flows from a spur tucked under its hind feet.

SOURCE

The bird-like qualities implied by its Latin name, Ornithorhynchus anatinus, include webbed feet, a flat bill similar to a duck’s, and the gene sequences that determine sex. Whereas humans have two sex chromosomes, platypuses have 10, the study showed.

“It is much more of a melange than anyone expected,” commented Ewan Birney, who led the genome analysis at the European Bioinformatics Institute in Cambridge.

The animal also possesses a feature unique to monotremes — an order including a handful of egg-laying mammals — called electroreception.

With their eyes, ears and nostrils closed, platypuses rely on sensitive electrosensory receptors tucked inside their bills to track prey underwater, detecting electrical fields generated by muscular contraction.

“By comparing the platypus genome to other mammalian genomes, we’ll be able to study genes that have been conserved throughout evolution,” said senior author Richard Wilson, a researcher at Washington University.

In captivity, platypuses have lived up to 17 years of age.

In the wild, they feed on worms, insect larvae, shrimps and crayfish, eating up to 20 percent of their body weight every day.

Males grow to a length of 50 centimetres (20 inches) and weigh about two kilos (4.5 pounds), with females about 20 percent shorter and lighter.

The genome sequenced for the study belongs to a female specimen from New South Wales nicknamed Glennie and can be accessed at www.ncbi.nih.gov/Genbank.

Stephen Barr, a molecular virologist in the Department of Medical Microbiology and Immunology, says his team has A team of researchers at the University of Alberta has discovered a gene that is able to block HIV, and in turn prevent the onset of AIDS.

“When we put this gene in cells, it prevents the assembly of the HIV virus,” said Barr, a postdoctoral fellow. “This means the virus cannot get out of the cells to infect other cells, thereby blocking the spread of the virus.”

Barr and his team also prevented cells from turning on TRIM22 – provoking an interesting phenomenon: the normal response of interferon, a protein that co-ordinates attacks against viral infections, became useless at blocking HIV infection.

“This means that TRIM22 is an essential part of our body’s ability to fight off HIV. The results are very exciting because they show that our bodies have a gene that is capable of stopping the spread of HIV.”

One of the greatest challenges in battling HIV is the virus’ ability to mutate and evade medications. Antiretroviral drugs introduced during the late 1990s interfere with HIV’s ability to produce new copies of itself – and even they are beneficial, the drugs are unable to eradicate the virus. Barr and his team have discovered a gene that could potentially do the job naturally.

“There are always newly emerging drug-resistant strains of HIV so the push has been to develop more natural means of blocking the virus. The discovery of this gene, which is natural in our cells, might provide a different avenue,” said Barr. “The gene prevents the assembly of the virus so in the future the idea would be to develop drugs or vaccines that can mimic the effects of this gene.”

“We are currently trying to figure out why this gene does not work in people infected with HIV and if there is a way to turn this gene on in those individuals,” he added. “We hope that our research will lead to the design of new drugs, or vaccines that can halt the person-to-person transmission of HIV and the spread of the virus in the body, thereby blocking the onset of AIDS.”

The researchers are now investigating the gene’s ability to battle other viruses.

Barr’s research is funded by the Canadian Institutes of Health Research, the Natural Sciences and Engineering Research Council and the Alberta Heritage Foundation for Medical Research. The findings are published in the Public Library of Science Pathogens.
SOURCE

By using a process called whole organ decellularization, scientists from the University of Minnesota Center for Cardiovascular Repair grew functioning heart tissue by taking dead rat and pig hearts and reseeding them with a mixture of live cells. The research will be published online in the January 13 issue of Nature Medicine.

“The idea would be to develop transplantable blood vessels or whole organs that are made from your own cells,” said Doris Taylor, Ph.D., director of the Center for Cardiovascular Repair, Medtronic Bakken professor of medicine and physiology, and principal investigator of the research.

Nearly 5 million people live with heart failure, and about 550,000 new cases are diagnosed each year in the United States. Approximately 50,000 United States patients die annually waiting for a donor heart.

While there have been advances in generating heart tissue in the lab, creating an entire 3-dimensional scaffold that mimics the complex cardiac architecture and intricacies, has always been a mystery, Taylor said.

It seems decellularization may be a solution – essentially using nature’s platform to create a bioartifical heart, she said.

Decellularization is the process of removing all of the cells from an organ – in this case an animal cadaver heart – leaving only the extracellular matrix, the framework between the cells, intact.

After successfully removing all of the cells from both rat and pig hearts, researchers injected them with a mixture of progenitor cells that came from neonatal or newborn rat hearts and placed the structure in a sterile setting in the lab to grow.

The results were very promising, Taylor said. Four days after seeding the decellularized heart scaffolds with the heart cells, contractions were observed. Eight days later, the hearts were pumping.

“Take a section of this ‘new heart’ and slice it, and cells are back in there,” Taylor said. “The cells have many of the markers we associate with the heart and seem to know how to behave like heart tissue.”

“We just took nature’s own building blocks to build a new organ,” said Harald C. Ott, M.D., co-investigator of the study and a former research associate in the center for cardiovascular repair, who now works at Massachusetts General Hospital. “When we saw the first contractions we were speechless.”

Researchers are optimistic this discovery could help increase the donor organ pool.

In general, the supply of donor organs is limited and once a heart is transplanted, individuals face life-long immunosuppression, often trading heart failure for high blood pressure, diabetes, and kidney failure, Taylor said.

Researchers hope that the decellularization process could be used to make new donor organs. Because a new heart could be filled with the recipient’s cells, researchers hypothesize it’s much less likely to be rejected by the body. And once placed in the recipient, in theory the heart would be nourished, regulated, and regenerated similar to the heart that it replaced.

“We used immature heart cells in this version, as a proof of concept. We pretty much figured heart cells in a heart matrix had to work,” Taylor said. “Going forward, our goal is to use a patient’s stem cells to build a new heart.”

Although heart repair was the first goal during research, decellularization shows promising potential to change how scientists think about engineering organs, Taylor said.

“It opens a door to this notion that you can make any organ: kidney, liver, lung, pancreas – you name it and we hope we can make it,” she said.

Researchers of the Center for Cardiovascular Repair team were assisted in their study by researchers from the University of Minnesota Department of Biomedical Engineering, who helped analyze data.

The study was funded by the Medtronic Foundation Endowment and a faculty research development grant from the University of Minnesota Academic Health Center.

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Researchers removed DNA from donated human eggs, and replaced it with DNA from the skin cells of two volunteers.

They produced embryos with genetic material that matched the men’s, but did not go on to extract stem cells.

UK experts say the research, published in the journal Stem Cells, is a small but not a great step forward.

The team at Stemagen Corporation in La Jolla, California, says the work could be an important stage in developing embryonic stem cells for patients.

The group produced five embryos called blastocysts from 25 donated eggs. DNA fingerprinting proved that at least one of these was a clone.

“We’re the first in the world to take adult human cells and then document that in fact we were able to clone embryos from them,” lead researcher Dr Samuel Wood told the BBC.

He said the embryos were destroyed in the process of verifying they were clones, but they were now working on creating stem cell lines.

Dr Lyle Armstrong of Newcastle University is one of a handful of other researchers who have made cloned human embryos using a technique known as nuclear transfer pioneered in Dolly the sheep. Unlike the US team, the Newcastle group used DNA from embryonic rather than mature tissue.

Dr Armstrong said the US study showed that the objective of using cells from an adult person to make individual stem cells might one day be possible.

“It’s a small step but not a great step forward,” he told BBC News. “It’s interesting that they’ve been able to repeat somatic cell nuclear transfer and get embryos of the stage where embryonic stem cells could be derived, but it is disappointing that they’ve failed to derive a stem cell line.”

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Whether the maternal or paternal copy gets switched on in such cases seems to be random. But the result could have a big impact on disease susceptibility and other biological traits.

It had been thought that there are only a handful of situations in which just one of a pair of gene copies is used. But a new screen of 4,000 human genes has uncovered 371 that sometimes play favourites, suggesting that this phenomenon is far more pervasive than had been thought. This kind of selective gene expression could create an extra source of variation between people, even when some of their genes are identical. “I like the idea that we’re all mosaics, and this might contribute to differences,” says Steve Henikoff, a biologist at the Fred Hutchinson Cancer Research Center in Seattle, Washington.

NATURE

They discovered that a single mutation in a gene is what determines whether people repeat their mistakes.

The mutation, the researchers say, leaves people with lesser D2 receptors in the brain that are activated when levels of the neurotransmitter dopamine drop. Dopamine is not only responsible for signalling fun and pleasure in the brain, but the neurotransmitter also helps in learning.

Klein and Ullsperger theorised that since dopamine is a chemical treat that urges the brain to repeat a choice if it is pleasurable, if not, then D2 receptors should be activated so that people don’t make the same mistake.

The researchers then tested this on a group of 26 men, twelve of whom had the gene mutation for low numbers of D2 receptors.

As a part of the study the subjects were shown sets of two symbols on a computer screen, and were asked to select one. The choice was followed by either a smiley face or a frown flashing on the screen.

The researchers then tested to check whether the men had learnt to choose the symbol that was the most positively reinforced and avoid the one that was the most negatively reinforced.

According to Science 1, they found that men with fewer D2 receptors had trouble avoiding their mistakes, reports Nature.

Brain imaging then used confirmed that the region called the rostral cingulate zone was involved in learning from mistakes. This particular region was found to be more active in the volunteers with normal D2 levels during the learning sessions, compared to those with the D2 mutation.

A brain region key to forming memories, the hippocampus, was also more active in the volunteers with normal D2 levels. (ANI)

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